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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >S0CS1 is an inducible host factor during HIV-1 infection and regulates the intracellular trafficking and stability of HIV-1 Gag
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S0CS1 is an inducible host factor during HIV-1 infection and regulates the intracellular trafficking and stability of HIV-1 Gag

机译：S0CS1是HIV-1感染期间的诱导型宿主因子，可调节HIV-1 Gag的细胞内运输和稳定性

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摘要

Human immunodeficiency virus type 1 (HIV-1) utilizes the macro-molecular machinery of the infected host cell to produce progeny virus. The discovery of cellular factors that participate in HIV-1 replication pathways has provided further insight into the molecular basis of virus-host cell interactions. Here, we report that the suppressor of cytokine signaling 1 (SOCS1) is an inducible host factor during HIV-1 infection and regulates the late stages of the HIV-1 replication pathway. SOCS1 can directly bind to the matrix and nucleocapsid regions of the HIV-1 p55 Gag polyprotein and enhance its stability and trafficking, resulting in the efficient production of HIV-1 particles via an IFN signaling-independent mechanism. The depletion of SOCS1 by siRNA reduces both the targeted trafficking and assembly of HIV-1 Gag, resulting in its accumulation as perinuclear solid aggregates that are eventually subjected to lysosomal degradation. These results together indicate that SOCS1 is a crucial host factor that regulates the intracellular dynamism of HIV-1 Gag and could therefore be a potential new therapeutic target for AIDS and its related disorders.
机译：1型人类免疫缺陷病毒（HIV-1）利用受感染宿主细胞的大分子机制生产后代病毒。参与HIV-1复制途径的细胞因子的发现为病毒-宿主细胞相互作用的分子基础提供了进一步的见识。在这里，我们报告说，细胞因子信号传导1（SOCS1）的抑制剂是HIV-1感染过程中的诱导宿主因子，并调节HIV-1复制途径的后期。 SOCS1可以直接结合到HIV-1 p55 Gag多蛋白的基质和核衣壳区域，并增强其稳定性和运输，从而通过独立于IFN信号传导的机制有效生产HIV-1颗粒。 siRNA对SOCS1的消耗减少了HIV-1 Gag的靶向运输和组装，导致其以核周固体聚集体的形式积累，最终被溶酶体降解。这些结果共同表明，SOCS1是调节HIV-1 Gag细胞内活力的重要宿主因子，因此可能成为艾滋病及其相关疾病的潜在新治疗靶标。

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